[40] Spectrophotometric detection of lipid conjugated dienes

Recknagel, Richard O.; Glende, Eric A.

doi:10.1016/s0076-6879(84)05043-6

Cited by 428 publications

(186 citation statements)

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“…The difference spectrum between the oxidized and unoxidized sample showed a K band near 233 nm, confirming that the increase in 233 nm absorption was imputable to conjugated-diene formation [10]. A secondary absorption maximum was also recorded, due to ketone dienes, in the region 260-280 nm [10]. Conjugated dienes were also assayed after Fe2--induced oxidation of liposomes.…”

Section: Measurement Of Lipid Peroxidationmentioning

confidence: 59%

Heparin protection against Fe²⁺‐and Cu²⁺‐mediated oxidation of liposomes

et al. 1996

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Heparin (HE) exhibited a protective effect on liposome peroxidation induced by Fe 2+ and Cu 2+, decreasing the formation of both conjugated dienes and thiobarbituric acid reactive substances (TBARS) in a dose-dependent manner. The antioxidant activity was more relevant in the oxidizing system employing Fe 2+ and H202 and generating the highly reactive "OH radical. The analysis of liposome size distribution by quasielastic laser light scattering showed that: (1) the native structure of the particles was completely lost after exposure to Fenton reagent; (2) the presence of HE in the reaction mixture completely prevented the peroxidative damage on liposomes. Thus, HE acts as an antioxidant factor on membrane lipid bllayer. This suggests that HE, released from mast-cell granules during inflammatory processes, might locally protect the cell membrane from the oxidative injuries.

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Section: Measurement Of Lipid Peroxidationmentioning

confidence: 59%

Heparin protection against Fe²⁺‐and Cu²⁺‐mediated oxidation of liposomes

et al. 1996

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“…Total lipid was extracted from liver tissue homogenates using the method of Bligh and Dyer, 23 and conjugated dienes were assessed spectrophotometrically by measuring the optical density between 220 and 300 nm. 24 Thiobarbituric Acid-Reactive Substances Determination. Liver thiobarbituric acid reactive substances (TBARS) were measured as described previously.…”

Section: Methodsmentioning

confidence: 99%

Increased lipid peroxidation and impaired antioxidant enzyme function is associated with pathological liver injury in experimental alcoholic liver disease in rats fed diets high in corn oil and fish oil

et al. 1998

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Increased hepatic oxidative stress with ethanol administration is hypothesized to be caused either by enhanced pro-oxidant production or decreased levels of antioxidants or both. We used the intragastric feeding rat model to assess the relationship between hepatic antioxidant enzymes and pathological liver injury in animals fed different dietary fats. Male Wistar rats (5 per group) were fed ethanol with either medium-chain triglycerides (MCTE), palm oil (PE), corn oil (CE), or fish oil (FE). Control animals were fed isocaloric amounts of dextrose instead of ethanol with the same diets. The following were evaluated in each group: liver pathology, lipid peroxidation, manganese superoxide dismutase (MnSOD) levels, copper-zinc SOD (CuZnSOD) levels, glutathione peroxidase (GPX) levels, and catalase (CAT) levels. All enzymes were evaluated using activity assays and immunoblots. Rats fed FE showed the most severe pathology (fatty liver, necrosis, and inflammation), those fed CE showed moderate changes, those fed PE showed fatty liver only, and those fed MCTE were normal. Parameters indicative of lipid peroxidation (conjugated dienes and thiobarbituric acid-reactive substances) were also greater in rat livers from animals fed the diets high in polyunsaturated fatty acids (CE and FE). CuZnSOD, GPX, and CAT activities showed an inverse correlation (r ‫؍‬ ؊.92, P F .01) with severity of pathological injury, with the lowest levels for both enzymes found in FE-fed rats. Decreased enzyme activity in CE-and FE-fed rats was accompanied by similar decreases in immunoreactive protein. Ethanol administration did not cause significant decreases in enzyme activity in groups that showed no necroinflammatory changes (MCTE and PE). MnSOD activity showed no significant change in any ethanol-fed group. Our results show that decreases in CuZnSOD, GPX, and CAT occur in rats showing pathological liver injury and also having the highest levels of lipid peroxidation. These results suggest that feeding dietary substrates that enhance lipid peroxidation can exacerbate both ethanol-induced oxidative damage as well as necroinflammatory changes. The decrease in activity of antioxidant enzymes observed in animals fed diets high in polyunsaturated fatty acids and ethanol could possibly increase the susceptibility to oxidative damage and further contribute to ethanol-induced liver injury. (HEPATOLOGY 1998;27:1317-1323.)

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“…The estimation showed a similar profile as compared with TBARS producof LP-related diene conjugation was made essentially as described tion, but in a lesser magnitude ( Table 2). The increased presby Recknagel and Glende, 16 and production of free radicals by the ence of diene conjugation found in the whole homogenate was subcellular fractions was determined by a technique based on lumipractically confined to plasma membrane. Microsomes also nol chemiluminiscence.…”

Section: In Addition Increased Lp Was Found In Microsomal Andmentioning

confidence: 99%

Selective enhancement of lipid peroxidation in plasma membrane in two experimental models of liver regeneration: Partial hepatectomy and acute CCl₄administration

1996

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with the rate of mitosis in several tissues, which has been It has been proposed that lipid peroxidation (LP) supported by the decreased LP found in subcellular fractions might be a modulator of cell division, influencing initiaof liver tumor cells. [2][3][4] However, some discrepancies have been tion and cessation of mitosis in regenerating liver. Howraised concerning the LP status during the characteristic acever, the understanding of the participating role of this tive cell proliferation following partial hepatectomy (PH). Acevent in the onset of liver proliferation has been hamtually, it was reported that both nicotinamide-adenine dinupered by the fact that both higher or lower LP have been cleotide phosphate-and tert-butyl hydroperoxide-induced reported after two-thirds partial hepatectomy (PH).LP were diminished after PH. [5][6][7] However, other research Therefore, the present study deals with the extent of LP groups have found an early increase of LP in homogenates in the main subcellular fractions from rat liver at early of regenerating liver. 8,9 Moreover, a transient enhancement stages of regeneration, induced by either PH of 70% or of mitochondrial LP has been reported to occur in preparaacute CCl 4 administration. Our results, using several tions obtained from hepatectomized rats. 10 methods to monitor LP, indicate a differential effect inThe present study was aimed at providing additional data the peroxidative pattern of specific subcellular fractions to settle the controversy about LP status during liver regenerfrom regenerating liver after 24 hours of PH: a decrease ation. We used two models to induce liver cell proliferation: in microsomes and an increase confined to plasma memtwo-thirds hepatectomy and acute intoxication with CCl 4 ; brane and cytosolic fractions, peaking after 24 hours of assessing LP by three different methods. The results show PH. In CCl 4 -treated rats, higher LP was also noted in that, in both models, an increased amount of LP activity is plasma membrane and cytosol, being maximal at the confined to the plasma membrane and cytosolic fractions, replicative stage in this experimental model (48 hours).whereas microsomes had a lower LP rate only in PH rats. In addition, increased LP was found in microsomal andThe changes in LP pattern, associated to liver regeneration, nuclear fractions, declining before the 48 hours. In hepashowed an organ specificity and correlated with the magnitectomized rats, changes in LP seem to be an organ-spetude of the loss of hepatic mass. The overall data suggest that cific event and related to only PHs capable of triggering controlled peroxidative modifications of membranes could be a synchronized proliferative response, namely above playing a role in the early steps of liver regeneration. fed ad libitum, and maintained under a 12-hour light/dark period. Surgical procedures were performed between 9 and 10 AM. Shamoperated animals were laparotomized under ether anesthesia to proThe liver is capable of recovering from damage or loss up vide a cont...

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[40] Spectrophotometric detection of lipid conjugated dienes

Cited by 428 publications

References 6 publications

Heparin protection against Fe²⁺‐and Cu²⁺‐mediated oxidation of liposomes

Heparin protection against Fe²⁺‐and Cu²⁺‐mediated oxidation of liposomes

Increased lipid peroxidation and impaired antioxidant enzyme function is associated with pathological liver injury in experimental alcoholic liver disease in rats fed diets high in corn oil and fish oil

Selective enhancement of lipid peroxidation in plasma membrane in two experimental models of liver regeneration: Partial hepatectomy and acute CCl₄administration

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[40] Spectrophotometric detection of lipid conjugated dienes

Cited by 428 publications

References 6 publications

Heparin protection against Fe2+‐and Cu2+‐mediated oxidation of liposomes

Heparin protection against Fe2+‐and Cu2+‐mediated oxidation of liposomes

Increased lipid peroxidation and impaired antioxidant enzyme function is associated with pathological liver injury in experimental alcoholic liver disease in rats fed diets high in corn oil and fish oil

Selective enhancement of lipid peroxidation in plasma membrane in two experimental models of liver regeneration: Partial hepatectomy and acute CCl4administration

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Heparin protection against Fe²⁺‐and Cu²⁺‐mediated oxidation of liposomes

Heparin protection against Fe²⁺‐and Cu²⁺‐mediated oxidation of liposomes

Selective enhancement of lipid peroxidation in plasma membrane in two experimental models of liver regeneration: Partial hepatectomy and acute CCl₄administration